Background: Cardiovascular diseases (CVD) are the primary cause of death in women in developed countries. CVD risk increases with age and further accentuates after the onset of menopause in women. This finding suggests that menopause accelerates the progression of pathogenesis of CVD independent of chronological age. Eating habits also play an important role in the development of CVD. However, their role in attenuating the risk for CVD in menopausal women is not clear. The purpose of this thesis is to investigate the associations between eating habits and cardiometabolic risk factors in menopausal women.
Methods: The thesis is based on the data of the Estrogenic Regulation of Muscle Apoptosis (ERMA) study, a population-based cohort study in which 47-55-year-old women (N=6878) were classified into premenopausal, perimenopausal, and postmenopausal groups based on follicle stimulating hormone (FSH) concentrations and bleeding patterns. A total of 918 women had completed data on eating
habits and cardiometabolic biomarkers. Eating habits were surveyed using a structured questionnaire, which included information regarding eating frequency and regularity. Blood serum concentrations of the total cholesterol, LDL-cholesterol (LDL-C) and HDL-cholesterol (HDL-C), triglycerides and fasting blood glucose were selected as cardiometabolic risk factors for the analysis. Differences in eating habits and cardiometabolic risk factors among menopausal groups were investigated by one-way analysis of variance (ANOVA) and a χ2-test. The associations between eating habits and cardiometabolic risk factors were investigated using Pearson’s correlation analysis and multiple linear regression. Finally, a sum variable was formed with dichotomous variables based on cardiometabolic risk factors’ reference values. The associations of eating habits with the sum variable were investigated by multinomial logistic regression.
Results: No statistically significant differences were observed in eating habits among menopausal groups. The cholesterol values, on the other hand, varied between the groups. Total cholesterol, LDL-C and HDL-C were the highest in the postmenopausal group (p<0.001), when compared to pre- and perimenopausal groups. Eating frequency was weakly and inversely associated with total cholesterol (r=-0.092, p<0.01) and LDL-C (r=-0.089, p<0.01). The associations remained even after adjustments for menopausal status, the BMI and age. However, the postmenopausal status was a stronger determinant of total cholesterol (β=0.540, p<0.001) and LDL-C (β=0.364, p<0.001) concentrations than eating frequency. Eating regularity was weakly and positively associated with triglycerides (r=0.073, p<0.05). In the linear regression model, the BMI (β=0.051, p<0.001) was a stronger determinant of the triglyceride concentrations compared to eating regularity, menopausal status and age. Multinomial regression model showed that women in postmenopause had a 2.42-fold higher risk of accumulation of three or more cardiometabolic risk factors than women in premenopause. A lower eating frequency of <4 meals per day was associated with the accumulation of three or more cardiometabolic risk factors (OR=1.64, p=0.048) as well.
Conclusions: Eating behavior was associated with cardiometabolic risk factors. However, menopausal status was a stronger determinant of the accumulation of cardiometabolic risk factors. Nonetheless, longitudinal studies are needed to better understand the associations with eating behavior and cardiometabolic risk factors in menopausal women.
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